The proposed experiments will be performed to understand further the metabolic and physiological mechanism(s) by which trigonelline, a plant hormone, promotes natural cell arrest in B2 of the cell cycle as root cells mature and assume a physiological function. Experiments are proposed to (1) determine if polyamines and inhibitors/augmentors of poly(ADP-ribose) synthesis affect the ability of trigonelline to promote G2 arrest, (2) determine, if inhibitors/augmentors of poly(ADP-ribose) influence the durations of the cell cycle phases, (3) determine if the relative labeling of poly(ADP-ribose) from 14C-NAD is influenced by trigonelline, cytokinins, polyamines of other chemicals that govern the proportion of cells in G1 or in B2, (4) determine if the rate and the extent of incorporation of 14C-NAD into other pyridine nucleotide pathway members is similar to other tested pyridine intermediates. These experiments are directed at trying to understand further the mechanisms by which natural substances regulate natural cell proliferation. The presence or absence of poly(ADP-ribosyl)ation on animal chromosomes has been implicated with cell arrest either in G1 or G2 phase of the cell cycle. Does Trigonelline, a natural G2 promoter, do so by varying poly(ADP-ribosy1)ation? Many compounds that affect the ability of trigonelline to promote cell arrest in G2, also affect the synthesis of poly(ADP-ribose) in a particular way. Does a correlation exist between the presence or absence of poly(ADP-ribosyl)ation and cell arrest either in G1 or in G2 phase of the cell cycle? By focusing on experiments that address the involvement of poly(ADP-ribose), on the cell cycle will we hope to gain insight as to how a natural hormone like trigonelline regulates the cell cycle?